Nickel-induced Heart Rate Variability Mediated Through Oxidative Stress and Inflammation in Spontaneously Hypertensive Rats

Chuen-Chau Chang (1,2), Tzu-Wei Hsueh (1), Jing-Shiang Hwang (3), TSUN-JEN CHENG (1)

(1) National Taiwan University, (2) Taipei Medical University Hospital, (3) Academia Sinica, Taipei, Taiwan

     Abstract Number: 45
     Last modified: October 8, 2009

Abstract
Particulate matter (PM) associated heart rate variability (HRV) alterations have been reported. However, the underlying mechanisms remain unclear. It is proposed that PM-induced HRV is mediated through oxidative stress and inflammation. The objective of this study is to determine whether alterations of HRV are mediated through oxidative stress and inflammation in spontaneously hypertensive (SH) rats treated with nickel sulfate (NiSO4). HRV changes in Wistar Kyoto (WKY) rats administered with NiSO4 (526micro-g) by intratracheal instillation was used as a reference to compare with those in SH rats treated with NiSO4 alone or in combination with N-acetylcysteine (NAC; 50 mg/Kg) or Celecoxib (5 mg/kg). Data via radiotelemetry were collected for 72h after exposure. Effects on 5-minute average of normal-to-normal intervals (ANN), natural logarithm transformed standard deviation of the normal-to-normal intervals (LnSDNN), and root mean square of successive differences of adjacent normal-to-normal intervals (LnRMSSD) were analyzed using self-control experimental designs. After NiSO4 exposure, SH rats had greater ANN change than WKY rats (p<0.05). After three doses of NAC and Celecoxib treatment, the alterations of ANN on SH rats were reduced to the levels produced in WKY rats. The LnRMSSD changes also had similar trend. However, the alteration of LnSDNN was less consistent among these experimental groups. In summary, nickel-induced HRV changes may be mediated through oxidative stress and inflammation. Since Ni is only one of components of ambient PM, more studies are needed to investigate whether other components of PM also induce changes of HRV through oxidative stress or inflammation.